Triple-negative breast cancer

Triple-negative breast cancer is an aggressive and heterogeneous triple negative breast cancer subtype defined by absence of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2, making it a major focus of proteomic biomarker discovery and precision medicine. Proteomic signatures and protein-based biomarkers are being explored for diagnosis, prognosis, and prediction of chemotherapy response, while multi-omics studies are refining its molecular stratification. Recent work also highlights therapeutic vulnerabilities and immunotherapy strategies, including PARP-1 inhibitor discovery, pembrolizumab-based neoadjuvant treatment, and nanoparticle-enabled photochemodynamic or biomimetic immune modulation. Mechanistic studies implicate C15ORF48-driven mitochondrial ROS regulation in chemotherapy resistance, NET-positive tumor-associated neutrophils in prognosis, and NY-ESO-1 overexpression as an immunotherapeutic target. Overall, the literature emphasizes both the clinical aggressiveness of triple negative breast cancer and the rapid expansion of biomarker-guided and immune-based interventions.

Biomarkers and prognosis

  • Proteomic signatures were reviewed as diagnostic, prognostic, and therapeutic biomarkers in triple negative breast cancer. (PMID:41512917)
  • Protein-based biomarkers were proposed to predict chemotherapy response and disease progression, with proteomics used to identify them. (PMID:41512917)
  • A six-gene panel derived from NET-positive tumor-associated neutrophils was identified as a reliable diagnostic biomarker for survival in triple negative breast cancer. (PMID:41671779)
  • NET-positive tumor-associated neutrophils were linked to prognosis and tumor progression in triple negative breast cancer. (PMID:41671779)

Resistance and molecular mechanisms

  • C15ORF48 up-regulation in a basal cell subpopulation contributed to chemotherapy resistance in triple negative breast cancer. (PMID:41931605)
  • The study on residual disease after AC treatment examined mechanisms of resistance to neoadjuvant chemotherapy in triple negative breast cancer. (PMID:41931605)
  • CDK16 dysregulation and overexpression were associated with poor prognosis in this aggressive breast cancer subtype. (PMID:41940903)
  • Relief of IDO1-mediated immunosuppression enhanced immunotherapeutic efficacy against triple negative breast cancer. (PMID:41949057)

Immunotherapy and targeted treatment

  • Neoadjuvant pembrolizumab-based therapy was evaluated in early-stage triple negative breast cancer, with immune-related adverse events studied as predictors of pathological complete response. (PMID:42011533)
  • NY-ESO-1 was found to be overexpressed and clinically relevant in triple negative breast cancer, supporting immunotherapeutic implications. (PMID:41846058)
  • Engineered Bacillus Calmette-Guérin mediated immunotherapy was developed for triple negative breast cancer. (PMID:41949057)
  • Fragment-based drug design with AI/ML enabled identification of novel PARP-1 inhibitors against triple negative breast cancer. (PMID:41724073)

Nanomedicine and combination therapy

  • Copper peroxide nanoparticles were used for CDT/PDT-synergized immunotherapy against aggressive triple negative breast cancer. (PMID:41525757)
  • Genetically engineered cellular membrane-camouflaged nanoparticles amplified immune response against recurrent metastatic triple negative breast cancer. (PMID:41633299)
  • MOF-based arginine nanocarriers were tested for coordinated immunometabolic and antitumor modulation in triple negative breast cancer. (PMID:42029068)
  • A gene-thermal feedback nanoplatform achieved greater than 93% tumor inhibition in triple negative breast cancer models. (PMID:41774834)